to its cause, and the mechanism of its production, it appears that the situation, as far at least as the ultimate solution of the problem is concerned, remains clouded.

Many theories have been advanced, since the work of Crile in 1903, each of which has both its exponents and opponents, owing chiefly to the inability of any one theory to meet all the conditions involved in the complex phenomenon known as surgical shock. So, at the present writing, it does not appear, from the data at hand, that the final solution of the problem has been reached.

Summarily speaking we recognize five principal theories as to the origin of shock.

1. Vasomotor exhaustion and paralysis (Crile, Mummery).

2. Cardiac spasm and eventual failures (Boise).

3. Inhibition of the functions of all the organs (Meltzer). 4. Acapnia or deficiency of CO2 in the blood (Yandall Henderson).

2

5. Morphologic changes in the nervous system (Gray and Parsons).

That no one of these is adequate is shown; 1. By the researches of Seelig and Joseph and of Seelig and Lyon who show that the vasomotor center is not paralyzed in shock and that the arteries are contracted.

2. W. G. Porter and F. G. Mann have demonstrated that stimulation of a nerve trunk, even when prolonged, fails to cause its complete exhaustion.

3. Mann has also shown that degenerative changes in the central nervous system are the result and not the cause of shock.

4. That inhibition of the function of all organs has been

refuted by the resuscitation of shocked, exsanguinated animals by transfusion.

5. Wainwright and also Short have rendered the heartspasm theory impossible by demonstrating the excellent recovery of the heart in shock by the operation of transfusion.

6. While Short demonstrates that acapnia is not usually present in surgical shock and therefore can only be depended on to explain a few cases.

Clinically shock may be divided into, first, anaphylactic shock, which is a laboratory phenomenon, more of academic than of practical importance. Second, toxic shock which differs in no way from surgical shock, except etiologically, with which its symptoms and disturbances are identical. Third, surgical shock. This condition irrespective of its etiology and the mechanism of its production, is undoubtedly vasomotor, an essential feature of which is a radical disturbance in blood-pressure, probably due to an interference in the normal distribution in the blood. Janeway and Jackson have shown experimentally that this disturbance is of such a character that the normal quota of blood upon the arterial side of the circulation is diminished, and that this diminution is maintained so that, as a consequence, even after the original cause of the disturbed distribution of the blood, whether of a mechanical, toxic or inhibitory nature, is removed, the abnormal distribution of the blood upon the arterial side of the circulation may not only persist but, in fatal cases, continues until death.

Much experimental work tends to sustain the theory that the low pressure found in shock is due to the retention of blood within the vessels on the venous side of the

circulation, particularly of the splanchnic areas, whereby the volume of blood in the arterial tree is reduced to such a degree that it mechanically interferes with the normal systole which even the contracted arterioles and small arteries, that have been demonstrated to exist during shock, fail to relieve.

C. F. Mann explains the loss of circulatory fluid in a different way, although the end-results are the same; namely, a reduced systolic and a diminished pulse pressure.

He believes "that the clinical signs of shock which appear after section of the abdomen and exposure of the viscera are due to a loss of circulatory fluid. This loss of fluid is not dependent on any primary impairment of the medullary center and takes place at a point beyond the control of the vasomotor mechanism. The causes for this loss of fluid are apparently the same as those which determine the accumulation of fluid in any other irritated area and produce the signs of inflammation. The nervous system probably plays no greater part in the former case than in the latter."

This diminution of the volume of the circulating blood offers an explanation of most of the acknowledged facts. It solves the crucial problem of a low blood-pressure with constricted arteries, vigorous heart muscle and an active vasomotor center. The changes in the nerve cells are due to the failure of the proper blood-supply and the mental apathy is the result of the same. The small pulse and pale skin are just what we should expect in such a condition. The undoubted value of saline infusion into a vein or injection into the rectum also receives explanation.

H. P. Fairlie has reported some practical conclusions

drawn from a study of the reaction of cases in shock under chloroform and under ether.

The fall in pressure in shock under ether is as great as the fall under chloroform, while the response is slower. In severe cases of shock at the end of the operation, the blood-pressure shows a better response under chloroform than it does under ether.

After weighing all considerations Fairlie suggests that in the severe cases chloroform is the anesthetic of choice, but that the anesthesia should be first induced by ether and then carried on by chloroform. The value of these conclusions must stand alone, as I have been unable to find any other references on either side of the question.

BIBLIOGRAPHY

1. F. S. Lee, Harvey Lectures, 1905-06, 169.

2. W. G. Porter, Am. Jour. Physiol., 1907-08, xx, 399, 444, 500. 3. Seelig and Lyon, Jour. A. M. A., Jan. 2, 1909, lii, pp. 45, 48. 4. Gray and Parsons, Brit. Med. Jour., April and May, 1912. 5. Pope, Calif. State Jour. Med., 1913, xi, 499.

6. H. P. Fairlie, Lancet, Feb. 28, 1914, i, 4722.

7. Janeway and Ewing, Ann. Surg., 1914, lix, 158.

8. F. G. Mann, Johns Hopkins Bull., 1914, xxiv, 205.

9. Seelig, Surg. Gyn. and Obstet., 1914, xviii, Abstra., p. 117.

10. Short, Brit. Jour. Surg., 1914, i, 114.

11. Seelig and Joseph, Proc. Soc. Exper. Biol. and Med., 1914, xii, 49.

12. Wainwright, Penna. Med. Jour., December, 1914, xviii, 3.

13. C. F. Mann, Surg. Gyn. and Obstet., 1915, xxi, 430.

14. Mann, Surg. Gyn, and Obstet., 1915, xxi, 430.

15. Morrison and Hooker, Amer. Jour. Physiol., 1915, April.

16. H. H. Janeway and H. C. Jackson, Proc. Soc. Exper. Biol. and Med., 1914 and 1915, xii, 193.

CHAPTER XXI

THE BLOOD-PRESSURE TEST IN OBSTETRICS

The universal employment of the sphygmomanometer and the routine study of normal and pathologic cases of pregnancy, during the past decade, have established a number of working rules which now serve as guides in diagnosis and prognosis, so that the sphygmomanometer now ranks with urinalysis in the examination of the pregnant.

In the blood-pressure test we have a most valuable means of detecting early toxemias, which often lead to the eclamptic state. Abnormal blood-pressure readings are one of the earliest indications of a departure from normal metabolism in the pregnant. This change may be evident before the development of any physical signs, or of any noticeable change in the urine. From a pathologic standpoint, it is evident that the close relation between the kidney and blood-pressure should be a valuable guide during this condition, since alterations in metabolism, the retention of waste products and the development of special toxins in the blood usually show themselves in a gradually rising blood-pressure, the one exception to this rule being those toxemias of hepatic origin in which the blood-pressure usually is not elevated (see page 392). These cases are, however, so few that they do not detract from the value and importance of the blood-pressure examination.

Routine blood-pressure observations should be made a part of the periodic examination during pregnancy.